Non-random chromosome abnormalities have been identified in human myelogenous leukemia, both chronic and acute. Although the relatively consistent association of the Philadelphia (Ph1) chromosome with chronic myelogenous leukemia (CML) has been recognized since 1960, the fact that it is the result of a translocation, usually to No. 9, was reported only in 1973. We have now identified a new consistent chromosome aberration associated with a specific type of leukemia, namely a translocation of the end of the long arm of No. 17 to the end of the long arm of No. 15 in patients with acute promyelocytic leukemia (APL). The use of reverse (R) banding indicates that the break in No. 15 is in q25 or q26, and in No. 17 is at the junction of q21 and q22 or is in q22. Nonrandom chromosome changes are also seen in myeloid cells of patients with leukemia following treatment of malignant lymphomas. Nine of ten such patients were missing a B group chromosome, identified as a No. 5 in eight. Sufficient data are available to determine not only which intact chromosomes are gained or lost in various myeloproliferative disorders, but to identify the specific regions that are affected. An analysis of the clonal chromosome aberrations in bone marrow cells that resulted in trisomy for all or part of No. 1 has revealed that all 34 patients included in the study were trisomic for bands 1q25 to 1q32. This consistency was noted despite the fact that these patients had a variety of hematologic disorders. The analysis of similar data for structural rearrangements of other chromosomes will reveal which portions of the chromosome usually are present in excess or are deficient, and which sites of the chromosome are most frequently involved in breaks. These data can then be combined with our increasing knowledge of the human gene map to determine whether there is a consistent association between particular classes of genes and the non-random abnormalities seen in human hematologic malignancies. This, in turn, may supply information as to which genes provide aneuploid cells with their proliferative advantage.